In modern intensive care units (ICUs), among other clinical settings, a vast and varied amount of physiological data is measured and collected, with the intent of providing clinicians with detailed information about the physiological state of each patient. The data include measurements from the bedside monitors of heavily instrumented patients, imaging studies, laboratory test results, and clinical observations. The clinician's task of integrating and interpreting the data, however, is complicated by the sheer volume of information and the challenges of organizing it appropriately. This task is made even more difficult by ICU patients' frequently-changing physiological state.
In these settings, several cardiovascular variables are used clinically to assess the performance of the heart as an effective pump. Chief among them are arterial blood pressure, cardiac output, total peripheral resistance, ventricular end-diastolic volume and pressure, contractility, and ejection fraction (all defined below).
Cardiac output (CO) is the amount of blood the heart pumps out over a unit of time. Typical values of CO in resting adults range from 3 liters/minute to 6 liters/minute. One basis for estimating or measuring CO is the formula:CO=HR×SV  (EQ. 1)where SV is cardiac stroke volume and HR is heart rate. If SV is measured in liters/beat and HR is measured in beats per minute, then CO is given in liters/minute, although any other units of volume and time may be used. Another basis for estimating or measuring CO is:CO=MAP/TPR  (EQ. 2)where MAP is mean arterial blood pressure (Arterial blood pressure is ABP) and TPR is total peripheral resistance.
End-diastolic volume (EDV) is the volume in the ventricle at the end of the ventricular filling phase of the cardiac cycle. End-systolic volume (ESV) is the volume in the ventricle at the end of the ejection phase of the cardiac cycle.
Stroke volume (SV) of the heart or of the left or right ventricle may be defined as the difference between end-systolic volume and end-diastolic volume, namely:SV=EDV−ESV  (EQ. 3)
Ejection fraction (EF) is defined as the ratio of the stroke volume (SV) to the ventricular end-diastolic volume (EDV) and is expressed in percent, namely:EF=SV/EDV=(EDV-ESV)/EDV  (EQ. 4)
More simply, EF represents the percentage of the end-diastolic volume in a ventricular chamber that is ejected per beat. EF can be measured in the right ventricle (RV) or the left ventricle (LV). Thus, RVEF is right ventricular ejection fraction and LVEF is left ventricular ejection fraction.
In this application, embodiments are presented with respect to the left ventricle, for which Applicants sometimes write EF instead of LVEF. The methods and systems described herein can easily be extended to the right ventricle.
Cardiac contractility is a measure of ventricular elastance at the end of the ejection. Contractility is usually thought of as being a measure of ventricular elastance for the left ventricle, i.e., cardiac contractility and left-ventricular contractility are equivalent terms in the art.
Chronically elevated end-diastolic pressures and volumes indicate poor pump performance, as do low states of contractility and a reduced ejection fraction [1]. (Numbers in square brackets refer to the reference list included herein. The contents of all these references are incorporated herein by reference.) Cardiac output and Total Peripheral Resistance can also be indicators of poor cardiovascular system performance. Ideally, these variables should be measured non- to minimally invasively for establishing initial diagnoses and tracked continuously for monitoring of disease progression and titration of therapeutic interventions.
The current clinical gold-standard measurements for measuring these variables, however, are costly, require expert operators, and are only performed intermittently. For instance, cardiac blood volumes are commonly measured echocardiographically: a skilled operator performs intermittent ultrasonic evaluations of the heart during which the relevant cardiac volumes are determined. Cardiac ejection fraction is then calculated from the resultant end-systolic and end-diastolic volumes.
Of particular relevance in clinical settings (e.g., in the ICU or the emergency room, ER) is the problem of distinguishing between three types of circulatory shock [which can be thought of as severe hypotension—or dangerously low mean arterial blood pressure or MAP], which may include, among others, septic shock (due to infections in the systemic vasculature), cardiogenic shock (relating to heart (pump) failure associated with myocardial infarction, cardiomyopathy, cardiac tamponade, etc.), hypovolemic shock (relating to low blood volume, e.g., as a consequence of bleeding or hemorrhage), anaphylactic shock (relating to circulatory shock due to a severe allergic reaction).
In ICUs or ERs, clinical interventions for each of these types of circulatory shock are different. In the case of hypovolemic shock, for example, one would try to increase a patient's blood volume, perhaps with a saline infusion or other appropriately-chosen fluid replacement therapy. With cardiogenic shock, on the other hand, one would try to reduce the load on the heart (either the inlet (preload) or outlet (afterload) pressures acting on the patient's heart), perhaps by administering drugs that would reduce the patient's vascular resistance or increase cardiac contractility. For patients with sepsis, intravenous fluid administration and/or medications that increase MAP by increasing TPR may be given.
The therapeutic interventions given to patients for circulatory shock or low MAP can often be incorrect if the relevant clinical information is not available. For instance, for patients with CHF, one would attempt diuresis (say, by giving a diuretic drug such as furosemide (‘Lasix’) to reduce the preload on the heart and remove any water that may have accumulated in the lungs (a condition known as pulmonary edema). On the other hand, for patients with hypovolemia, one would give the patient a bolus of fluid, e.g., saline infusion, in an attempt to increase distending blood volume, and in turn, MAP. If one were to give a patient with CHF a fluid bolus, this would worsen the preload on the heart and probably worsen the patient's pulmonary edema symptoms [3].
Currently, it is quite difficult to determine the root cause of a patient's shock, mainly for two reasons. First, CO, EF, and LVEDV are not frequently measured in the ICU. Of these, CO can be measured with relative ease once a pulmonary artery catheter is in place, but this is an invasive procedure that is reserved for the sickest of patients [3]. Second, for many ICU patients, there is always the possibility that the shock is a result of multiple organs failing, i.e., they may he suffering from heart failure and a systemic infection.
Thus, methods and apparatus for effectively establishing initial differential diagnoses for circulatory shock, and for continuous monitoring of the disease progression are needed. Such methods would greatly facilitate the monitoring, diagnosis, and treatment of cardiovascular disease.
The statements in this section merely provide background information related to the present disclosure and may not constitute prior art